Diseases in plants cause considerable crop loss from year to year resulting both in economic deprivation to farmers and additionally in many parts of the world to shortfalls in the nutritional provision for local populations. The widespread use of fungicides has provided considerable security against plant pathogen attack. However, despite $1 billion worth of expenditure on fungicides, worldwide crop losses amounted to approximately 10% of crop value in 1981 (James, 1981; Seed Sci. & Technol. 9: 679–685).
The severity of the destructive process of disease depends on the aggressiveness of the pathogen and the response of the host. One aim of most plant breeding programs is to increase the resistance of host plants to disease. Typically, different races of pathogens interact with different varieties of the same crop species differentially, and many sources of host resistance only protect against specific pathogen races. Furthermore, some pathogen races show early signs of disease symptoms, but cause little damage to the crop. Jones and Clifford (1983; Cereal Diseases, John Wiley) report that virulent forms of the pathogen are expected to emerge in the pathogen population in response to the introduction of resistance into host cultivars and that it is therefore necessary to monitor pathogen populations. In addition, there are several documented cases of the evolution of fungal strains which are resistant to particular fungicides. As early as 1981, Fletcher and Wolfe (1981; Proc. 1981 Brit. Crop Prot. Conf.) contended that 24% of the powdery mildew populations from spring barley, and 53% from winter barley showed considerable variation in response to the fungicide triadimenol and that the distribution of these populations varied between varieties with the most susceptible variety also giving the highest incidence of less susceptible types. Similar variation in the sensitivity of fungi to fungicides has been documented for wheat mildew (also to triadimenol), Botrytis (to benomyl), Pyrenophora (to organomercury), Tapesia (to MBC-type fungicides) and Mycosphaerella fijiensis to triazoles to mention just a few (Jones and Clifford; Cereal Diseases, John Wiley, 1983).
Cereal species are grown world-wide and represent a major fraction of world food production. Although yield loss is caused by many pathogens, the necrotizing pathogens Septoria and Tapesia are particularly important in the major cereal growing areas of Europe and North America (Jones and Clifford; Cereal Diseases, John Wiley, 1983). In particular, the differential symptomology caused by different isolates and species of these fungi make the accurate predictive determination of potential disease loss difficult. Consequently, the availability of improved diagnostic techniques for the rapid and accurate identification of specific pathogens will be of considerable use to field pathologists.
The eyespot disease of cereals is caused by the fungi Tapesia yallundae and Tapesia acuformis is restricted to the basal culm of the plant. The two causal pathogens were previously classified as two subspecies of Pseudocercosporella herpotrichoides (Fron) Deighton (anamorph). T. yallundae refers to the variety herpotrichoides and the SF-,L-,I- or W-types. T acuformis corresponds to the variety acuformis and the FE-, N-, II- or R-types (Leroux and Gredt, 1997; 51:321–327). Wheat, rye, oats and other grasses are susceptible to the eyespot disease which occurs in cool, moist climates and is prevalent in Europe, North and South America, Africa and Australia. Wheat is the most susceptible cereal species, but isolates have been identified which are also virulent on other cereals. The R-strain (T. acuformis) of the fungus, for example, has also been isolated from rye and grows more slowly on wheat than the W-strain (T. yallundae) which has been isolated from wheat. Although eyespot may kill tillers or plants outright, it more usually causes lodging and/or results in a reduction in kernel size and number. Yield losses associated with eyespot are of even greater magnitude than those associated with Septoria tritici and Septoria nodorum. Typical control measures for eyespot include treatment with growth regulators to strengthen intemodes, and fungicide treatment. However, the differing susceptibility of cultivars to different strains of the fungus render the predictive efficacy of fungicide treatments difficult. In addition, both Leroux et al (1997; Pesticide Science, 51:321–327) and Dyer et al (2000; Appl. and Environ. Microbiol. 66:4599–4604) have reported on isolates of T. yallundae with reduced sensitivity to the imidazole DMI fungicide prochloraz (1-[N-propyl-N-[2-92,4,6-trichlorophenoxy)ethyl]carbamoyl]-imidazole). Following heavy treatments of benzimidazole fungicides such as benomyl, carbendazim and thiabendazole, acquired resistance to this class of fungicides was determined in both T. acuformis and T. yallundae (Leroux and Cavelier, 1983; Phytoma 351:40) and (Cavelier et al, 1985; Bull. OEPP 85:495).
Thus, there is a real need for the development of technology which will allow the identification of specific races of pathogen fungi which are resistance to certain fungicides early in the infection process. By identifying the specific race of a pathogen before disease symptoms become evident in the crop stand, the agriculturist can assess the likely effects of further development of the pathogen in the crop variety in which it has been identified and can choose an appropriate fungicide if such application is deemed necessary.